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Published in: Current Dermatology Reports 4/2018

Open Access 01-12-2018 | Immunology (D Lee, Section Editor)

Immunology of Wound Healing

Authors: Samantha Ellis, Elaine J. Lin, Danielle Tartar

Published in: Current Dermatology Reports | Issue 4/2018

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Abstract

Purpose of Review

Chronic wounds are a tremendous burden on the healthcare system and lead to significant patient morbidity and mortality. Normal cutaneous wound healing occurs through an intricate and delicate interplay between the immune system, keratinocytes, and dermal cells. Each cell type contributes signals that drive the normal phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This paper reviews how various immunological cell types and signaling molecules influence the way wounds develop, persist, and heal.

Recent Findings

Concurrent with the achievement of hemostasis, neutrophils are the first cells to migrate to the wound bed, brought in by pro-inflammatory signals including IL-8. Their apoptosis and engulfment by macrophages (efferocytosis) provides a key signal to the local immune milieu, including macrophages, to transition to an anti-inflammatory, pro-repair state, where angiogenesis occurs and granulation tissue is laid down. Myofibroblasts, activated through contractile forces and signaling molecules, then drive remodeling, where granulation tissue becomes scar. Unchecked inflammation at this stage can result in abnormal scar formation.

Summary

Although the derangement of immune signals at any stage can result in impaired wound healing, recent research has shown that the key transition point lies between the inflammatory and the proliferative phases. This review summarizes the events that facilitate this transition and discusses how this process can be disrupted, leading to chronic, non-healing wounds.
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Metadata
Title
Immunology of Wound Healing
Authors
Samantha Ellis
Elaine J. Lin
Danielle Tartar
Publication date
01-12-2018
Publisher
Springer US
Published in
Current Dermatology Reports / Issue 4/2018
Electronic ISSN: 2162-4933
DOI
https://doi.org/10.1007/s13671-018-0234-9

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